ArticleInfection and immunity2005
Variations in Helicobacter pylori lipopolysaccharide to evade the innate immune component surfactant protein D.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 59 citations in OpenAlex.
- Strategies ofFrontiers in cellular and infection microbiology · 2024Review
- Sweet impersonators: Molecular mimicry of host glycans by bacteria.Glycobiology · 2022Review
- Small RNA mediated gradual control of lipopolysaccharide biosynthesis affects antibiotic resistance in Helicobacter pylori.Nature communications · 2021Article
- Galectin-2 Has Bactericidal Effects againstInternational journal of molecular sciences · 2020Article
- A Newly Discovered Drug Resistance GeneInfection and drug resistance · 2019Article
- Helicobacter pylori modulates host cell responses by CagT4SS-dependent translocation of an intermediate metabolite of LPS inner core heptose biosynthesis.PLoS pathogens · 2017Article
- Metabolic labelling of cholesteryl glucosides inChemical science · 2016Article
- Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori.Infection and immunity · 2016Article
- Surfactant Protein D Binds to Coxiella burnetii and Results in a Decrease in Interactions with Murine Alveolar Macrophages.PloS one · 2015Article
- Structural modifications of Helicobacter pylori lipopolysaccharide: an idea for how to live in peace.World journal of gastroenterology · 2014Review
- Antiadhesive properties of arabinogalactan protein from ribes nigrum seeds against bacterial adhesion of Helicobacter pylori.Molecules (Basel, Switzerland) · 2014Article
- Antiadhesive properties of Abelmoschus esculentus (Okra) immature fruit extract against Helicobacter pylori adhesion.PloS one · 2014Article
- Implication of antigenic conversion of Helicobacter pylori lipopolysaccharides that involve interaction with surfactant protein D.Infection and immunity · 2012Article
- Surfactant protein D (Sp-D) binds to membrane-proximal domain (D3) of signal regulatory protein α (SIRPα), a site distant from binding domain of CD47, while also binding to analogous region on signal regulatory protein β (SIRPβ).The Journal of biological chemistry · 2012Article
- Effect of Helicobacter pylori cdrA on interleukin-8 secretions and nuclear factor kappa B activation.World journal of gastroenterology · 2012Article
- Outer membrane biogenesis in Escherichia coli, Neisseria meningitidis, and Helicobacter pylori: paradigm deviations in H. pylori.Frontiers in cellular and infection microbiology · 2012Review
- Lipoarabinomannan localization and abundance during growth of Mycobacterium smegmatis.Journal of bacteriology · 2011Article
- Role of glycan synthesis in colonization of the mammalian gut by the bacterial symbiont Bacteroides fragilis.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Helicobacter pylori induces an antimicrobial response in rhesus macaques in a cag pathogenicity island-dependent manner.Gastroenterology · 2008Article
- Lipopolysaccharide diversity evolving in Helicobacter pylori communities through genetic modifications in fucosyltransferases.PloS one · 2008Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is a common and persistent human pathogen of the gastric mucosa. Surfactant protein D (SP-D), a component of innate immunity, is expressed in the human gastric mucosa and is capable of aggregating H. pylori. Wide variation in the SP-D binding affinity to H. pylori has been observed in clinical isolates and laboratory-adapted strains. The aim of this study was to reveal potential mechanisms responsible for evading SP-D binding and establishing persistent infection. An escape variant, J178V, was generated in vitro, and the lipopolysaccharide (LPS) structure of the variant was compared to that of the parental strain, J178. The genetic basis for structural variation was explored by sequencing LPS biosynthesis genes. SP-D binding to clinical isolates was demonstrated by fluorescence-activated cell sorter analyses. Here, we show that H. pylori evades SP-D binding through phase variation in lipopolysaccharide. This phenomenon is linked to changes in the fucosylation of the O chain, which was concomitant with slipped-strand mispairing in a poly(C) tract of the fucosyltransferase A (fucT1) gene. SP-D binding organisms are predominant in mucus in vivo (P = 0.02), suggesting that SP-D facilitates physical elimination. Phase variation to evade SP-D contributes to the persistence of this common gastric pathogen.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.